ArticleFree radical biology & medicine2019
Glutathione deficiency-elicited reprogramming of hepatic metabolism protects against alcohol-induced steatosis.
Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Characterizing the metabolomes of microglia, astrocytes and neurons in ageing and Alzheimer's brains.Nature cell biology · 2026Article
- Article
- The Role of Methylmalonic Acid in the Risk of Sarcopenia and All-Cause Mortality Among Individuals With Sarcopenia: Evidence From NHANES.Food science & nutrition · 2025Article
- Reduced Glutathione Promoted Growth Performance by Improving the Jejunal Barrier, Antioxidant Function, and Altering Proteomics of Weaned Piglets.Antioxidants (Basel, Switzerland) · 2025Article
- Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency.Chemico-biological interactions · 2024Article
- Preparation, Structural Identification, and Screening of Egg-Derived Peptides with Facilitating Alcohol Metabolism Activity.Foods (Basel, Switzerland) · 2024Article
- Critical Roles of the Cysteine-Glutathione Axis in the Production of γ-Glutamyl Peptides in the Nervous System.International journal of molecular sciences · 2023Review
- Hepatoprotective Effect of Albumin Peptide Fractions from Corn Germ Meal against Alcohol-Induced Acute Liver Injury in Mice.Foods (Basel, Switzerland) · 2023Article
- Persistence of improved glucose homeostasis in Gclm null mice with age and cadmium treatment.Redox biology · 2022Article
- Review
- Novel approaches to liver disease diagnosis and modeling.Translational gastroenterology and hepatology · 2021Review
- A Study onEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Could protein content of Urinary Extracellular Vesicles be useful to detect Cirrhosis in Alcoholic Liver Disease?International journal of biological sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Depletion of glutathione (GSH) is considered a critical pathogenic event promoting alcohol-induced lipotoxicity. We recently show that systemic GSH deficiency in mice harboring a global disruption of the glutamate-cysteine ligase modifier subunit (Gclm) gene confers protection against alcohol-induced steatosis. While several molecular pathways have been linked to the observed hepatic protection, including nuclear factor erythroid 2-related factor 2 and AMP-activated protein kinase pathways, the precise mechanisms are yet to be defined. In this study, to gain insights into the molecular mechanisms underpinning the protective effects of loss of GCLM, global profiling of hepatic polar metabolites combined with liver microarray analysis was carried out. These inter-omics analyses revealed both low GSH- and alcohol-driven changes in multiple cellular pathways involving the metabolism of amino acids, fatty acid, glucose and nucleic acids. Notably, several metabolic changes were uniquely present in alcohol-treated Gclm-null mouse livers, including acetyl-CoA enrichment and diversion of acetyl-CoA flux from lipogenesis to alterative metabolic pathways, elevation in glutamate concentration, and induction of the glucuronate pathway and nucleotide biosynthesis. These metabolic features reflect low GSH-elicited cellular response to chronic alcohol exposure, which is beneficial for the maintenance of hepatic redox and metabolic homeostasis. The current study indicates that fine-tuning of hepatic GSH pool may evoke metabolic reprogramming to cope with alcohol-induced cellular stress.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.